hexokinase/نوبة

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Neonatal seizures in monkeys and rabbits: brain glucose depletion in the face of normoglycemia, prevention by glucose loads.

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Sustained convulsive seizures were induced with bicuculline in newborn rabbits and marmoset monkeys. In both species, seizures were predominantly tonic, with generalized polyspikes on the EEG. Brain glucose concentration fell dramatically during seizures in both species, and in many normoglycemic

Hexokinase redistribution in vivo.

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Heterogenous stock mice in addition to mice selectively bred to maximally differ in their severity of alcohol withdrawal seizures (withdrawal seizure-resistant (WSR) and withdrawal seizure-prone (WSP] were used to provide evidence in favor of the importance of the rapidly changing distribution of

Inhibition of hexokinase leads to neuroprotection against excitotoxicity in organotypic hippocampal slice culture.

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During seizures, glucose concentrations are high in the hippocampus. Mitochondrial hexokinase (HK) catalyzes the first essential step of glucose metabolism and directly couples extramitochondrial glycolysis to intramitochondrial oxidative phosphorylation. The neuroprotective effects of an HK

Dominant form of congenital hyperinsulinism maps to HK1 region on 10q.

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OBJECTIVE In a family with congenital hyperinsulinism (HI), first described in the 1950s by McQuarrie, we examined the genetic locus and clinical phenotype of a novel form of dominant HI. METHODS We surveyed 25 affected individuals, 7 of whom participated in tests of insulin dysregulation (24-hour

Asterixis and encephalopathy following metrizamide myelography: investigations into possible mechanisms and review of the literature.

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Marked asterixis occurred in two patients following metrizamide myelography. One also suffered generalized seizures and the other had severe stuttering speech for seven days. The spectrum of toxic manifestations of metrizamide is reviewed with emphasis on the unusual lethargy and other depressive

Biochemical changes during graded brain ischemia in gerbils. Part 1. Global biochemical alterations.

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In Mongolian gerbils (Meriones unguiculatus) cerebral ischemia was produced by occlusion of the right common and the left external carotid arteries. Gerbils were classified according to their neurological appearance as "symptom-negative" (8 animals), "mild symptoms" (unilateral hemiparesis, 10

Alterations in Cytosolic and Mitochondrial [U-13C]Glucose Metabolism in a Chronic Epilepsy Mouse Model.

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Temporal lobe epilepsy is a common form of adult epilepsy and shows high resistance to treatment. Increasing evidence has suggested that metabolic dysfunction contributes to the development of seizures, with previous studies indicating impairments in brain glucose metabolism. Here we aim to

On-line monitoring of extracellular brain glucose using microdialysis and a NADPH-linked enzymatic assay.

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A method to monitor extracellular glucose in freely moving rats, based on intracerebral microdialysis coupled to an enzyme reactor is described. The dialysate is continuously mixed with a solution containing the enzymes hexokinase and glucose-6-phosphate dehydrogenase, and the fluorescence of NADPH

Cerebral glucose and glycogen metabolism in diazinon-treated animals.

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The intraperitoneal (IP) treatment of rats with diazinon (40 mg/kg) resulted in a variety of changes in the brain. Glycogen was depleted, but there was an increase in the activities of glycogen phosphorylase, phosphoglucomutase, hexokinase, lactate dehydrogenase, and fructose 1,6 diphosphatase. The

Changes in cerebral glycogenolysis and related enzymes in diazinon treated hyperglycaemic animals.

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Effect of diazinon (10,20 and 40 mg/kg, i.p.) on the level of blood glucose in rats was investigated. Hyperglycaemia peaked 2 h after i.p. treatment with 40 mg/kg diazinon. The cerebral acetylcholinesterase activity was significantly reduced. The blood level of pyruvic acid was unchanged while that

Absence status epilepticus resulting from metrizamide and omnipaque myelography.

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Two cases of absence status are described, one case following metrizamide myelography and the other from omnipaque myelography. Metrizamide has been well known to cause convulsive seizures even in patients without epilepsy. The exact mechanism is not known but appears to be direct neuronal toxic

A new mouse model of GLUT1 deficiency syndrome exhibits abnormal sleep-wake patterns and alterations of glucose kinetics in the brain.

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Dysfunction of glucose transporter 1 (GLUT1) proteins causes infantile epilepsy, which is designated as a GLUT1 deficiency syndrome (GLUT1DS; OMIM #606777). Patients with GLUT1DS display varied clinical phenotypes, such as infantile seizures, ataxia, severe mental retardation with learning

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